{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T03:13:08Z","timestamp":1784257988408,"version":"3.55.0"},"reference-count":55,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T00:00:00Z","timestamp":1761436800000},"content-version":"vor","delay-in-days":55,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82173960"],"award-info":[{"award-number":["82173960"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31400302"],"award-info":[{"award-number":["31400302"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Excessive inflammatory response represents the primary pathological hallmark of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Helicobacter pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      ) gastritis. Toll\u2010like receptor 2 (TLR2) has emerged as a promising therapeutic target because of its crucial role in regulating inflammatory responses and tissue damage caused by\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      . Galangin (Gal), a naturally occurring flavone, possesses a variety of pharmacological activities, including anti\u2010inflammatory and antibacterial effects. This study systematically evaluates the therapeutic potential of Gal in\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      gastritis, with specific emphasis on elucidating its TLR2\u2010targeting mechanism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      An\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010induced mouse gastritis model was established to evaluate the therapeutic effects of Gal at dosages of 50 and 100\u2009mg\/kg\/day over a two\u2010week administration period. The\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">H. pylori<\/jats:styled-content>\n                        \u2010\n                      <\/jats:italic>\n                      infected GES\u20101 human gastric epithelial cells were utilized for mechanistic exploration. Molecular docking and siRNA transient transfection techniques were integrated to elucidate the specific interactions between Gal and TLR2.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Gal inhibited the proliferation of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      and alleviated the inflammation caused by\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      in both in\u00a0vitro and in\u00a0vivo. Furthermore, Gal inhibited the activation of the TLR2\/MyD88 signaling pathway, which suppressed the downstream phosphorylation of MAPK (p38\/JNK\/ERK) and NF\u2010\u03baB nuclear translocation. Notably, the knockdown of\n                      <jats:italic>TLR2<\/jats:italic>\n                      diminished the inhibitory effects of Gal on MyD88 expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Gal demonstrated effectiveness in ameliorating\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      gastritis through the therapeutic inhibition of TLR2. Further investigation is warranted to explore the combination of Gal with other\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      eradication treatments.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/hel.70084","type":"journal-article","created":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T03:33:16Z","timestamp":1761535996000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Galangin Alleviates\n                    <i>Helicobacter pylori<\/i>\n                    Gastritis Through\n                    <scp>TLR2<\/scp>\n                    Inhibition and Modulation of the\n                    <scp>MyD88<\/scp>\n                    \u2010Dependent Inflammatory Cascades"],"prefix":"10.1111","volume":"30","author":[{"given":"Wuyinxiao","family":"Zheng","sequence":"first","affiliation":[{"name":"Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine, School of Pharmacy Hubei University of Chinese Medicine  Wuhan People's Republic of China"},{"name":"Hubei Shizhen Laboratory  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zijian","family":"Zheng","sequence":"additional","affiliation":[{"name":"Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine, School of Pharmacy Hubei University of Chinese Medicine  Wuhan People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingyu","family":"Yang","sequence":"additional","affiliation":[{"name":"Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine, School of Pharmacy Hubei University of Chinese Medicine  Wuhan People's Republic of 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